Eshkevari Et Al. Investigate The Effects Of Electroacupunture In Cold Depression Case Study

1. Dr. Sapolsky’s research in the Masai Mara National Park of Kenya involved collecting blood samples from baboons to measure hormones involved in the stress response. After anaesthetizing the baboon in an unassuming way (to avoid hormones produced from anticipatory stress) he collected blood samples from their bodies.

Why Zebras Don’t Get Ulcers is a book about the physiology of stress. It gets into great detail about what exactly is going on inside the body during periods of high stress, and also what short and long term affects are caused by that stress. The first chapter give a brief description of each chapter in the rest of the book. Each subsequent chapter explains different stressors, levels of stress, and hormonal responses to stress. Many of the chapters also include research and discoveries on how stress affects the human body, many of which are somewhat recent discoveries, only occurring in the last one hundred years or so. Robert Sapolsky is able to explain to his readers much about the physiology of stress and how endocrinology plays the most

The biological purpose of the stress response is to help the body to survive either some sort of attack or a serious illness like a stroke or heart attack. During the stress response glucocorticoids divert the bodies energy to the areas necessary for survival like the muscles and the brain and it shuts down the areas that are not necessary for survival like the digestive and immune systems (Sopolsky, 2009). Chronic Stress in this context, is to experience this physical effect on regular or long term basis. This has become a public health issue for humans because we experience this chronic biological response on a too frequent a basis for psychological reasons (Stress, 2008).

Viewed from an evolutionary standpoint, in early times stress caused the stimulation of the sympathetic nervous system resulting in an outpouring of the hormones epinephrine, norepinephrine, and glucocorticoids that were essential to the life-preserving fight or flight reactions of primitive man (Anthony 1988). However, the nature of stress for the individual today is different. It is only occasionally and unexpectedly that one is confronted with overwhelming, life-threatening stresses. Present stresses arise from everyday stresses of work, finances and school. The problem is that the body still continues to respond in the same fashion as primitive times. This makes the large release of hormones very harmful. They can cause an increase in blood pressure, damage muscle tissue, lead to infertility, inhibit growth, damage the hippocampus and suppress the immune system (Carlson 1994). It is therefore, important that individuals learn to control the stresses in their lives. The more detrimental coping behaviors will cause a larger change

The aim of this study is to investigate the relationship between various psychological responses (mood, emotion and coping) and the sympathetic nervous system response to an acute stress challenge. This will help understand the underlying mechanisms in the stress-ill-health relationship and will increase the knowledge about how psychological aspects may reduce physiological responses. Therefore, the collected knowledge will help form future interventions.

One of the effects of this hormone is that it makes a person more inclined to go to a close family member or friend, as they want to be surrounded by people who care about their well-being. Additionally, it helps heal stress-induced damages to the heart. Essentially, stress makes a person social, as they crave physical contact and increase their empathy. The final study discovered that people who experience a major stressful event have an increased mortality rate; however, if they spend time helping other people, they experience no increase whatsoever. In conclusion, stress affects a person’s body in whatever manner they think it will: A person will remain healthy if they view it positively, but a person who views it negatively will be

The nervous, endocrine, and immune systems share a close relationship critical to maintaining homeostasis during psychological and immune stress (Carlsson, Anneli, Ludvigsson, & Faresjö, 2014). Chronic stress, primarily mediated by the glucocorticoid cortisol, is associated with deleterious health outcomes and immune deficiency. However, acute stress is associated with protective health effects and immune enhancement. Stress has generally been regarded as adaptive when acute and short-term but maladaptive when chronic (Dhabhar, 2006; Carlsson, Anneli, Ludvigsson, & Faresjö, 2014; Johnson, Riley, Douglas, & Riis, 2013; Flinn and England, 2003; Wiegers, Reul, Holsboer, & de Kloet, 1994).

The hormones released during the acute stress response is considered the “master switch” in controlling the person’s behavioral and physiological adaptation to stress. (Mannironi, et al., 2013) The targets of these hormones are the cognitive, wake sleep, and reward and fear centers of the brain. (Chrousos, 2009) The growth, gastrointestinal, cardiorespiratory, metabolic, reproductive and thyroid hormone axis, and immune systems are also effected. (Chrousos, 2009) Optimal basal

Firdaus Dhabhar gave a short lecture on August 19th, 2015 about the good effects that stress can have on our lives. I read two papers published by Dr. Dhabhar in the last five years, both concerning his research on the biological response of stress and how this can impact our daily lives as well as how it can be both detrimental and essential to good health. Each paper explored stress, one was more focused on the physical and the other focused on both the physical and the mental. Given my own project this summer, I was especially interested in the paper published by Aschbacher and colleagues in 2013 because they also explored cortisol reactivity to stress. While their project and my project looked at very different things in very different populations it was exciting to read more about cortisol and how people are exploring this hormone’s role in our stress

The title of this article does properly reflect the findings of this experiment because the results of this study are that hypothalamic progesterone is required for LH release and is important in the LH surge. This title also includes how the study animals were modified prior to experimentation and the name of the animals in this study. It is important to identify the study animal in the title of the article so that readers know that the experiments are conducted in a mammalian system and which hormones will be discussed in the article.

Long-term alterations in the secretion include a glutocorticoid hormones cortisol via the hypothalamus pituitary adrenal access personal play crucial role in mediating the link between chronic stress exposure and ability to variety of diseases. (Stalder et al. 2012) Some of the biological consequences of such arousal were first identified by Selye (1956) as the General Adaptation Syndrome. Selye noted t h a t a principal characteristic of this response is an elevation in cortisol level. As a result of this early work and of more recent laboratory-based research, cortisol is now often regarded a s a "stress hormone" and as an objective marker of stress (Baum et al., 1982). (Pollard 1995)Registering for stressors cognitive affective states

Upon activation by an emotional or physical stressor, corticotropic releasing hormone (CRH) is released from the paraventricular cells of the hypothalamus and exerts its effect on the anterior pituitary gland Here, CRH stimulates the synthesis of adrenocorticotropic hormone (ACTH) and its release into the bloodstream [19,20]. In turn, ACTH acts on receptors of the adrenal cortex to stimulate the synthesis and release of cortisol [19,20]. Also known as the body’s ‘‘stress hormone’’, cortisol travels through the blood in both protein-bound (inactive) and free (active) forms. Cortisol can act to limit its own synthesis via a negative feedback mechanism to the hypothalamus and pituitary gland [19,20]. Upon reaching a target cell, free cortisol diffuses through the cell membrane to bind to the cytoplasmic glucocorti- coid receptor [19,20]. This ligand-receptor complex translocates to the nucleus where it binds glucocorticoid-response elements to affect transcription of target genes [19,20]. As our body’s central glucocorticoid, cortisol has many actions. These include gluconeogenesis, lipolysis, modulating the immune system, increase of blood pressure and insulin resistance [19,20]. Cortisol is metabolized by 11-beta hydroxysteroid dehydrogenase type 2 to its inactive form, cortisone [19,20 GOW

For a better understanding when an animal (e.g., horse) becomes stressed, the hypothalamic-pituitary-adrenal (HPA) axis is activated resulting in heat production, as a result of increases in catecholamine and cortisol levels as well as blood flow responses. This will cause changes in heat production and loss from the animal. The HPA axis has a direct effect and interactions among the hypothalamus, the pituitary gland, and the adrenal glands. These interactions comprise the HPA axis, an essential part of the neuroendocrine system which regulates reactions to stress and controls many body processes, such as digestion, the immunity, emotions, sexuality, energy storage and expenditure (Dantzer and Mormède, 1983; McMillan, 2005; Von Borell et al., 2007), thus they can be termed as stressors (Minton, 1994; Bartolomé et al., 2013). Stress may be defined as the homeostatic, physiological and behavioral responses detectable in an animal as a kind of result of interactions with environmental stressors (Stephens, 1980; Bartolomé et al., 2013). More specifically, the sympatho-adrenal (ANS) medullary system consists of both sympathetic and parasympathetic nervous system, which is

An examination of the conditions endured by research animals beforehand can also be attributed to a source of conclusion inaccuracy between animal experimentation successes and clinical research failures. Stress, commonly experienced by animal subjects in a lab setting, is a major factor known for contaminating the accuracy and reliability of biomedical research results. Stress causes a chain reaction of heightened readings, such as increased heart rates, pulses, muscular actions, and hormonal balances. Executing experiments on a subject with misrepresentative vital signs can greatly skew the results and interpretations drawn from a study. Stress can be experienced in a variety of manners. Mice, for example, experience a reactive condition known as “sympathy pains” when in a laboratory setting. In addition to the individual response taken at the foreign sights, sounds, and smells, mice are affected by the stress level and anxiety experienced by other mice surrounding them. Like humans, mice can feel sympathy towards one another and react accordingly. Performing experiments on animals that suffer from an abnormal amount of stress will skew evidence collected, and make it difficult for scientists to reach conclusions about predicted similar human responses.

Long-term activation of this stress-response system can lead to the disruption of almost all of the body’s processes. If this happens, the individual has an increased risk of developing numerous health problems. So, to prevent this from happening, the problem must be nipped in the bud.